Not applicable.
1. Field of the Invention
The present invention relates generally to implantable cardiac devices, such as implantable cardioverter defibrillators (ICDs). The present invention more particularly relates to reducing ICD integrated circuit (IC) power consumption in such implantable cardiac devices.
2. Background Art
Implantable cardiac stimulation devices, such as implantable cardioverter defibrillators (ICDs), are well known in the art. Such devices may include, for example, implantable cardiac pacemakers and defibrillators either alone or combined in a common enclosure. The devices are generally surgically implanted in a pectoral region of the chest beneath the skin of a patient. The primary components of an ICD include a monitoring and detection mechanism, a capacitor, a battery, a sensing system for detecting an arrhythmia, and a control system for controlling delivery of a capacitive discharge electrical shock in response to a detected arrhythmia. The implantable devices generally function in association with one or more electrode carrying leads which are implanted within the heart. The electrodes are positioned within the heart for making electrical contact with the muscle tissue of their respective heart chamber. Conductors within the leads couple the electrodes to the device to enable the device to deliver the desired electrical therapy.
ICDs are often employed to monitor a patient""s heart to detect arrhythmias, which are irregular heartbeats that feature either very rapid ventricular contractions (tachycardia), an excessively slow heartbeat (bardycardia) or, most commonly, extra or xe2x80x9cprematurexe2x80x9d beats. The most common arrhythmia is atrial fibrillation, which is an abnormal rhythm of the heart that can result in an increased risk of stroke due to the formation of emboli (blood clots) in the heart. More specifically, atrial fibrillation is an abnormality of heart rhythm in which chambers of the heart no longer contract in an organized manner. Heart rate often becomes irregular and may be very fast, producing palpitations. Atrial fibrillation can lead to symptoms of heart failure (shortness of breath, edema, palpitations) and chest pains and, when left untreated, occasionally can lead to stroke.
The heart has a right side and a left side. Each side has a chamber that receives blood returning to the heart (an atrium) and a muscular chamber that is responsible for pumping blood out of the heart (a ventricle). Atria are relatively thin-walled chambers, whereas the ventricles are much more muscular. Blood passes from the atria into the ventricles through two processes. During the resting phase, when the ventricles are not contracting, the tricuspid and mitral valves open. Some of the blood that has accumulated in the atria passively flows through the tricuspid and mitral valves into the right and left ventricles, respectively. The atria then contract, pumping blood out and into the ventricles. Once the ventricles fill with blood, they contract, pumping blood out of the ventricles, into the lungs, and to the body.
Contractions of the different chambers of the heart are normally organized in a specific manner. An electrical impulse travels through the heart""s chambers and sets off contractions. The heart""s xe2x80x9cspark plugxe2x80x9d is a small area of specialized heart tissue called the SA node, located in the right atrium. Each time this tissue xe2x80x9cfires,xe2x80x9d an impulse travels first through the right and left atria, signaling these chambers to contract and pump blood into the ventricles, and then travels down into a patch of another specialized heart tissue located between the atria and the ventricles, called the AV node. Electrical-wire-like specialized tissue conducts the impulse down into the ventricles, where it signals the right ventricle to contract and to pump blood out and into the lungs, and signals the left ventricle to contract and pump blood out to the rest of the body. Normal sequence of electrical activation of the chambers of the heart is called normal sinus rhythm.
In atrial fibrillation, normal sinus rhythm does not occur. Instead, multiple xe2x80x9cwaveletsxe2x80x9d of electrical impulses travel randomly through the atria, leading to more or less random activation of different parts of the atria at different times. Because the tissues of the right and left atria are not stimulated to contract in an organized manner, the walls of the atria more or less quiver.
Lack of organized contraction by the atria causes several detrimental things to happen. First, because less blood is pumped into the ventricles, there is less blood circulating throughout the body and blood accumulates in the lungs, causing shortness of breath (dyspnea) and other symptoms of heart failure. Second, because the heart is no longer pumping blood into the ventricles, the blood in the atria (particularly in a small part of the left atrium, the left atrial appendage) becomes relatively stagnant. There is a small but real risk that, over time, the stagnant blood will form a blood clot. If a blood clot forms, it may eventually enter the left ventricle and then get pumped out into the body. If this happens, the clot may travel to the brain, block the flow of blood in a cerebral artery, and cause a stroke.
Third, atrial fibrillation can create chest pain (angina). Multiple disorganized wavelets of electrical activity bombard the AV node with electrical impulses. When a great many electrical impulses are conducted through the AV node down into the ventricles, the ventricles contract very rapidly, producing a very fast heart rate. When the ventricles contract too rapidly, less blood is pumped into the body and blood may xe2x80x9cback upxe2x80x9d into the lungs. Rapid contraction increases the ventricles"" demand for oxygen. The demand may exceed the ability of the coronary arteries to supply the ventricles with oxygen-rich blood, causing angina.
When an ICD detects an arrhythmia (e.g., due to atrial fibrillation), the ICD is often used to deliver an appropriate shock to the patient""s heart in an attempt to return the heart to normal sinus rhythm. Sometimes, second, third, and fourth (and possibly more) shocks are required in a critical case to return the heart to normal sinus rhythm.
Current ICDs are battery powered. The battery is implanted in the patient as part of the ICD. The types of batteries used in ICDs vary. Battery powered implantable medical devices require many years of continuous operation. Low power consumption is the most important criteria in designing the IC. It is very well known that reducing the supply voltage is one of the most effective ways to reduce power consumption. See, T. Burd, R. Brodersen, xe2x80x9cDesign Issues for Dynamic Voltage Scalingxe2x80x9d, IEEE Symposium on Low Power Electronics, Digest of Technical papers, pp 9-14, July 2000, and L. Wong, C. Kwok, G. Rigby, xe2x80x9cA 1-V CMOS D/A Converter with Multi-Input Floating-Gate MOSFETxe2x80x9d IEEE Journal of Solid States Circuits, pp. 1386-1390, October 1999. Lowering the operating voltage puts harder constraints on the analog circuits, as lower voltages are available to turn on the transistor. Low threshold voltage (Vth) processes have been developed to target low voltage operations. See, S. Bazarjani, W. Snelgrove, xe2x80x9cIV Switched-Capacitor xcexa3xcex94 Modulatorxe2x80x9d, IEEE Symposium on Low Power Electronics digest of tech papers, pp70-73, October 1995 and T. Adachi, et al, xe2x80x9cA 1.4V Switched-Capacitor Filter,xe2x80x9d Proc. IEEE CICC, pp8.2.1-8.2.4, May 1990. In addition, as devices shrink in the deep sub-micron processes, transistors are also expected to operate in low supply voltages in order to maintain long term reliability. The drawback of these low Vth or sub-micron processes is that they significantly increase the leakage current. This increase in leakage current has a very significant impact on switched-capacitor implementations of analog circuits.
Low power consumption is crucial for implantable medical devices. Reducing supply voltage is well known to minimize power dissipation. Transistor""s Vth are becoming lower, driven by low supply voltage and shrinking technology. However, low Vth transistors have high leakage currents which impact the performance of switched-capacitor circuits, sample and hold amplifiers, and more.
What is needed is a mechanism for reducing transistor leakage current in such a way that power dissipation is minimized and supply voltage is reduced.
The present invention addresses the common problem seen in switched-capacitor circuits as a result of transistor leakage current. The new technique can significantly minimize the effective leakage current to regain circuit performance. This technique also achieves both minimal silicon area and low power operation. The new circuit technique of the invention largely minimizes the effective leakage current when the switch is turned off by employing an active feedback loop to automatically cancel both junction and sub-Vth channel leakage. This general technique of the invention can be used in many different circuit applications.